Author

H. G. Kasler

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell type annotation· 2 Research Focus:chromatin & epigenetic regulation· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1

Frequent Co-Authors

E. Verdin· 3 shared A. J. Covarrubias· 1 shared A. Kale· 1 shared A. McDonald· 1 shared A. Oliveira Pisco· 1 shared B. Schilling· 1 shared C. Brenner· 1 shared C. D. Wiley· 1 shared

Activity by Year

2017-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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3 shared papersImmunology

E. Verdin

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Author profile →

3 papers

Recent·Most cited

A Proposed Unified Mitotic Chromosome Architecture

J. Sedat, A. McDonald, H. G. Kasler, E. Verdin, H. Cang, M. Arigovindan, C. Murre, M. Elbaum

The paper proposes a unified molecular architecture for human Chromosome 10 throughout the mitotic cycle, based on interphase structure and validated by digital PCR.

bioRxiv · Oct 14, 2021Cell Biology

Aging-related inflammation driven by cellular senescence enhances NAD consumption via activation of CD38+ macrophages

A. J. Covarrubias, A. Kale, R. Perrone, J. A. Lopez-Dominguez, A. Oliveira Pisco, H. G. Kasler, M. S. Schmidt, C. D. Wiley, S. S. Iyer, N. Basisty, Q. Wu, R. Kwok, I. Heckenbach, K.-O. Shin, Y.-M. Lee, , E. Verdin

This study identifies CD38+ macrophages as a driver of NAD decline during aging through inflammation linked to cellular senescence in metabolic tissues.

bioRxiv · Jul 31, 2019Immunology

Histone Deacetylase 7 Mediates Tissue-Specific Autoimmunity via Control of Innate Effector Function in Invariant Natural Killer T-Cells

H. G. Kasler, I. S. Lee, H. W. Lim, E. Verdin

This study shows HDAC7 regulates NKT cell development and function, with its disruption leading to tissue-specific autoimmunity, particularly in hepatobiliary diseases.

bioRxiv · Oct 18, 2017Immunology